Papachristou Georgios I
World J Gastroenterol. 2008 Nov 7;14(41):6273-5. doi: 10.3748/wjg.14.6273.
Acute pancreatitis (AP) is a common and potentially lethal acute inflammatory process with a highly variable clinical course. It is still unclear why some patients progress to organ failure and others do not. Physicians, ability to predict which patients will develop severe disease is limited. Routine clinical and laboratory data and multi-factorial clinical scores measured on admission and during the first 48 h of hospitalization are currently the standards of care used to estimate the magnitude of the inflammatory response to injury. Current literature highlights several common environmental, metabolic and genetic factors that increase the risk of AP development and subsequent adverse sequelae. Several cytokines have been found to play a critical role in the pathogenesis of AP by driving the subsequent inflammatory response, to include tumor necrosis factor-alpha (TNF-alpha), Interleukin-1 (IL-1), IL-6 and monocyte chemotactic protein-1 (MCP-1). Large, prospective studies are still needed to address these questions by identifying AP risk factors and serum biomarkers of severe disease.
急性胰腺炎(AP)是一种常见且可能致命的急性炎症过程,其临床病程高度可变。目前尚不清楚为何有些患者会进展为器官衰竭而另一些患者则不会。医生预测哪些患者会发展为重症疾病的能力有限。常规临床和实验室数据以及入院时和住院最初48小时内测得的多因素临床评分是目前用于评估对损伤的炎症反应程度的标准治疗方法。当前文献强调了几种常见的环境、代谢和遗传因素,这些因素会增加AP发生及随后出现不良后遗症的风险。已发现几种细胞因子通过驱动随后的炎症反应在AP发病机制中起关键作用,包括肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、IL-6和单核细胞趋化蛋白-1(MCP-1)。仍需要开展大型前瞻性研究,通过识别AP危险因素和重症疾病的血清生物标志物来解决这些问题。